Associação da frequência alélica dos polimorfismos dos genes do sistema renina angiotensina com a força muscular e pressão arterial de idosas

Physiological changes induced by the aging process is dynamic and progressive, reducing the adaptability and independence of older people and may be influenced by genetic and environmental factors. Thus the aim of this thesis was to investigate the association between polymorphism of the ACE gene ID and the phenotypes of muscular strength and blood pressure of 62 elderly Brazilian (67.35 ± 5.66 years) during a 16-week program of supervised training. The elderly women were stratified by age, with the group 1 (G1, n = 34) <70 years and group 2 (G2 n = 28) ≥ 70 years, and in three groups by ACE, ACE-II (n = 8) ACE- DD (n = 35) and ACE-ID (n = 19). The level of muscle strength was evaluated by the method of maximum repetitions and measures of blood pressure (BP) were measured before and after training (PAPré1 and PAPós1) and before and after each training session (PAPre2 and PAPós2), in place of training. DNA samples were isolated from peripheral blood leukocytes polymorphism and insertion / deletion (ID) of the ACE gene (rs1800795) was genotyped by polymerase chain reaction (PCR) plus PCR-confirmatory. The genotype distribution of the polymorphism ID attended the prerogatives of Hardy-Weitíherg. There was variation in power levels before and after training and the age between groups (t-test) and the ACE polymorphism (ANOVA) (p <0.05). Depending on the results it was concluded that resistance training helps to reduce SBP and increased muscle strength of upper and lower limbs when considering the age and ACE polymorphism. In this study the Elderly carriers of the D allele were more reactive to changes in BP resistance training. This study was multidisciplinary project involving researchers in the areas Medical, Physical Education, Pharmacy, Nutrition, Gerontology and Statistics. This fulfilled the requirements of the multidisciplinary Graduate Program in Health Sciences

Efeitos da azilsartana sobre a doença periodontal em um modelo experimental com ratos wistar

Periodontal diseases, highly prevalent disease in worldwide population, manifest primarily in two distinct entities: plaque-induced gingivitis and periodontitis. Periodontitis is a chronic inflammatory disease characterized of different levels of collagen, cementum, and alveolar bone destruction. Recent experimental studies demonstrated anti-inflammatory and antirreabsortive effect of antihypertensive agents of the angiotensin II receptor blockers class on periodontal disease. The aim of this study was to evaluate the effects of azilsartan (AZT), a potent inhibitor of the angiotensin II receptor which has minimal adverse effects on bone loss, inflammation, and the expression of matrix metallo proteinases (MMPs), receptor activator of nuclear factor kB ligand (RANKL), receptor activator of nuclear factor kB (RANK), osteoprotegerin (OPG), cyclooxygenase-2 (COX-2), and cathepsin K in periodontal tissue in a rat model of ligature-induced periodontitis. Male Wistar albino rats were randomly divided into 5 groups of 20 rats each: (1) nonligated, water; (2) ligated, water; (3) ligated, 1 mg/kg AZT; (4) ligated, 5 mg/kg AZT; and (5) ligated, 10 mg/kg AZT. All groups were treated with water or AZT for 10 days. Periodontal tissues were analyzed by morphometric exam, histopathology and immunohistochemical detection of MMP-2, MMP-9, COX-2, RANKL, RANK, OPG, and cathepsin K. Levels of IL-1b, IL-10, TNF-a, myeloperoxidase (MPO), and glutathione (GSH) were determined by ELISA. Treatment with 5 mg/kg AZT resulted in reduced MPO (p˂0.05) and IL-1b (p˂0.05) levels and increased in Il-10 levels (p˂0.05). It was observed a reduced expression of MMP-2, MMP-9, COX-2, RANK, RANKL, cathepsin K, and a increased expression of OPG in the animals subjected to experimental periodontitis and threated with AZT (5 mg/kg). Conclusions: These findings suggest an anti-inflammatory and anti-reabsortive effects of AZT on ligature-induced periodontitis in rats.

Influência de mudanças de fase no ciclo claro-escuro sobre o controle autonômico cardíaco de ratos

Introduction: The circadian system has neural projections for the Autonomic Nervous System (ANS), directly interfering with sympathetic-vagal modulation of the cardiovascular system. Disturbances in the circadian system, such as phase changes in light-dark cycle (LD), has been related to the risk of development of cardiovascular diseases due to increased sympathetic tone and reduction o Heart Rate Variability (HRV - RR intervals). Purpose: Investigate the interaction between Circadian Timing System and cardiac autonomic control in rats. Materials and methods: We used 18 Wistar rats (♀, age = 139.9 ± 32.1 days, weight = 219.5 ± 16.2 g), divided into three distinct groups: Control (CG), phase delay of 6h (GDe) and phase advance of 6h (GAd). Three animals were excluded during data collection (CG/GDe/GAd - n=5). Telemeters were surgically implanted in each animal for continuous acquisition of electrocardiographic (ECG) signals (duration of 21 days in the CG and 28 days in GDe/ GAd). A LD cycle was established 12h: 12h, beginning of light at18:00h and dark at 06:00h. The animals remained in the same CG LD cycle throughout the experimental period, while, on the 14th day of registration, the GDe and GAd underwent a delay and an advance in 6h, respectively. Throughout the experimental period, the locomotor activity (LA), the mean heart rate (mHR) and variables related to iRR [mean RR (mRR), SDNN, RMSSD, LF, HF and LF/ HF ratio ] were recorded. All data were analyzed in blocks of 3 and 7 days, for the presence of circadian rhythm, values of Cosinor - mesor, amplitude and acrophase (paired t test), phase relationship, differences between light and dark (t test independent), averages every 30 minutes along each time series (two-way ANOVA with post hoc Bonferroni). The data block B1,M1 and M2 in CG served as benchmarks for comparisons between series of analysis of the GAT/GAV. Results: We observed circadian rhythmicity in the variables LA, mRR and mFC(p<0.01). mRR and mFC showed phase relationship with the LA in all three groups, being less stable in GAd. In the CG, no significant differences between blocks were found in any of the analyzes(p>0.05). Among the 7 day blocks, there was a significant reduction in mRR(p=0.04) and mFC(p=0.03) in GDe and significant reduction in HF mean(p=0.02) in GAd; and between 3 day blocks, a significant increase of LF/HF(p= 0.04) in the GDe; besides mRR(p=0.03), SDNN(p=0.04), RMSSD (p=0.04), LF (p=0.01) and HF(p=0.02) significant increase in the GAd. It was found that the differences between the means of the mRR, LA and mFC in light and dark phases were not significant after phase changes in some of the blocks/moments (GDe and GAd). No significant results were found when comparing rhythmic variables means every 30 minutes over the blocks, except for a significant decrease in mRR at the middle of the dark phase (B2) and the start of light phase (B3) - (p<0.01). Conclusion: phase advances and delays (6h) altered cardiac autonomic control in the experimental groups by temporarily HRV decrease. Phase advances apparently had greater negative interference in this process, in relation to the phase delays.

Influência do jet lag social em marcadores circadianos de atividade - repouso e cardíaco em estudantes de medicina

Studies reveal that in recent decades a decrease in sleep duration has occurred. Social commitments, such as work and school are often not aligned to the "biological time" of individuals. Added to this, there is a reduced force of zeitgeber caused by less exposure to daylight and larger exposure to evenings. This causes a chronic sleep debt that is offset in a free days. Indeed, a restriction and extent of sleep called "social Jet lag" occurs weekly. Sleep deprivation has been associated to obesity, cancer, and cardiovascular risk. It is suggested that the autonomic nervous system is a pathway that connects sleep problems to cardiovascular diseases. However, beyond the evidence demonstrated by studies using models of acute and controlled sleep deprivation, studies are needed to investigate the effects of chronic sleep deprivation as it occurs in the social jet lag. The aim of this study was to investigate the influence of social jet lag in circadian rest-activity markers and heart function in medical students. It is a cross-sectional, observational study conducted in the Laboratory of Neurobiology and Biological Rhythmicity (LNRB) at the Department of Physiology UFRN. Participated in the survey medical students enrolled in the 1st semester of their course at UFRN. Instruments for data collection: Munich Chronotype Questionnaire, Morningness Eveningness Questionnaire of Horne and Östberg, Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale, Actimeter; Heart rate monitor. Analysed were descriptive variables of sleep, nonparametric (IV60, IS60, L5 and M10) and cardiac indexes of time domain, frequency (LF, HF LF / HF) and nonlinear (SD1, SD2, SD1 / SD2). Descriptive, comparative and correlative statistical analysis was performed with SPSS software version 20. 41 students participated in the study, 48.8% (20) females and 51.2% (21) males, 19.63 ± 2.07 years. The social jet lag had an average of 02: 39h ± 00:55h, 82.9% (34) with social jet lag ≥ 1h and there was a negative correlation with the Munich chronotype score indicating greater sleep deprivation in subjects prone to eveningness. Poor sleep quality was detected in 90.2% (37) (X2 = 26.56, p <0.001) and 56.1% (23) excessive daytime sleepiness (X2 = 0.61, p = 0.435). Significant differences were observed in the values of LFnu, HFnu and LF / HF between the groups of social jet lag <2h and ≥ 2h and correlation of the social jet lag with LFnu (rs = 0.354, p = 0.023), HFnu (rs = - 0.354 , p = 0.023) and LF / HF (r = 0.355, p = 0.023). There was also a negative association between IV60 and indexes in the time domain and non-linear. It is suggested that chronic sleep deprivation may be associated with increased sympathetic activation promoting greater cardiovascular risk.